You need to get calories from somewhere, should it be from carbohydrate or fat?

Thursday, October 06, 2011

Adipocyte insulin resistance

It was in late 2007 that I first blogged about the concept of adipocyte insulin resistance and of course it is back in my mind while I work through ideas on metabolic flexibility and insulin resistance in general. It is a very simple concept that the fatter adipocytes become (using whatever delivery system you like, ASP if you must) the harder it becomes to push more fat in to them. And certainly the harder it becomes to keep it there once it is installed. So this idea of adipocyte insulin resistance limiting fat gain is very intuitive and probably correct. How big adipocytes can get is probably determined by how strong your pancreas is combined with how responsive your adipocytes are to insulin as they swell. A pancreas of steel and relatively insulin-resistance resistant (no typo) adipocytes combine to get you to the over 200kg mark. This came up in comments on the last post. Is this true?

A rather nice paper was published back in the 1960s showing this very clearly. I have seen it cited as purporting to show that elevated fasting insulin is a consequence of obesity, rather than a cause. This is a fascinating and rather counter intuitive concept, so you just have to go have a look see at the paper. Luckily it's free access.

It does show, very convincingly, that adipocyte size correlates with adipocyte insulin resistance on the adipocyte cellular level. I rather like that.

It also demonstrates quite clearly that forced, brutal adipocyte size reduction by a couple of months on a 600kcal/d diet improves adipocyte insulin sensitivity as adipocyte size shrinks.

There are two core concepts which need to be taken away from this paper.

The first is that as adipocytes swell they become progressively less able to respond to insulin. This obviously translates in to insulin resistance of adipocytes ultimately limiting fat gain within the limits of the pancreas to secrete or hypersecrete insulin. That is if you accept that insulin is in any way involved in fat storage.

Now. What does this mean for the carbohydrate hypothesis of fat gain?

It is the RESISTANCE of adipocytes to insulin which limits fat gain.

And the corollary is??? Sensitivity to insulin drives fat gain. You can't have one conclusion without the other.

Anyone telling you that adipocyte insulin resistance limits fat gain and yet insulin per se has nothing to do with fat gain... Well, you decide. I have.

Although the group measured many, many things the only information we get about fasting insulin levels and post challenge insulin levels are these five paired graphs:

There is nothing in the text or tables giving any numeric data about insulin levels in obese individuals and no details at all from the normal groups. I don't mind this too much as the study was really aimed at adipocyte size and adipocyte glucose metabolism in response to exogenous insulin. This was the main drive of the paper. Note that they didn't look at adipocyte beta oxidation, no one had any idea this might be compromised back in the 1960s, so we get no idea about the ability of adipocytes to carry out this essential function.

Look, fasting insulin in five obese people is not generally elevated, it's reported as being only slightly elevated in two out of the five obese patients. This obviously implies that elevated fasting insulin does not predict weight gain. There we go. Time to pack up and go home.

Ah yes, but which fasting insulin are we looking at? Remember that group of starved obese folk we chatted about previously who had three different fasting insulin levels? One level on their normal (obesogenic) diet, one on a calorie and carbohydrate limited diet and another on the full starvation non-diet (ie complete carbohydrate restriction): 45 or 38 or 15-20 microIU/ml.

In obese people (but not in people who have normal metabolic flexibility) you can simply dial fasting insulin by carbohydrate intake. The question we cannot answer from Hirsch's study is what the fasting (and the 24h AUC) insulin values were for the five obese participants while they were free living on their normal obesogenic (high carbohydrate, you can bet) diet and slowly gaining weight? Remember we only need an average of 5g/d adipose tissue accumulation for long term obesity.

We are given an insulin value during phase I on a weight stability diet with a carbohydrate intake fixed at 45% of not-quite-enough-for-comfort calories. This is not what a given individual would normally choose to eat. In real life these people would not be on a weight stable diet. They certainly would not have been limiting their carbohydrate to 45% of calories. So we have no idea what their fasting insulin level would have been before stabilisation on phase I, but is certainly going to have been higher than the graphs show.

After massive weight loss during phase II of the study (on 600kcal/d for several months, probably only bearable because carbohydrate was limited to around 50-55g/d and the doors were locked [jk!]) we go in to phase III and get our second set of curves. Here we are now maintaining weight stability at a markedly reduced body weight with a smaller portion size of a still 45% carbohydrate diet, so total carbohydrate intake will be a bit lower. Hence the slightly reduced fasting insulin... But of course none of this represents the life which led to the enrolment in the study.

Subjects will be hungry.

While ever they stay hungry and limit carbohydrate to 45% of their never-quite-enough calorie intake, their insulin levels will stay low and they will, hungrily, stay slim.

Four of the five patients managed this for quite some time. Kudos to them and their willpower. You have to wonder about the fifth patient. Lost to follow up? Not lost to follow up but fatter than pre study? Just got fed up with people sticking needles in their butt?

How effective for long term weight control is chronic caloric restriction? Answers on a postage stamp to...

Are these people fixed? Their adipocytes certainly have scope to respond better to insulin and will inhibit lipolysis more effectively than during obesity. This limits FFA leakage due to insulin resistance which decreases FFA delivery to muscles and so allows muscles to take up glucose better, so both glucose and insulin curves improve. But are they really, really fixed? Will they will simply regain their lost weight, unless they enjoy being hungry all the time? Especially if they increase their total carbohydrate intake? And why are they hungry? Another post in this series there.

Addendum: Running through the methods section of Petersen's paper it is actually worth noting that fasting insulin and simple derivatives of fasting insulin plus glucose, such as the HOMA score, are rather blunt instruments for picking up insulin resistance. The more complex insulin sensitivity index is better but even this failed to pick out two out of twelve apparently insulin sensitive participants who turned out to be insulin resistant on the hyperinsulinaemic clamp, the current gold standard for picking out insulin resistant subjects. So, while insulin resistance is core, simple fasting insulin has to be accepted as a blunt instrument. Clamps, unfortunately, are not simple to perform. End addendum.

Of course you cannot dial fasting insulin by carbohydrate intake in normal individuals. So all you have to do is include enough normal people in your longditudinal studies and there will be no significant correlation between fasting insulin and subsequent weight gain. What would you expect?

Anyhoo, back to adipocyte insulin resistance. Stretching adipocytes appears to have effects on their sensitivity to insulin. As adipocytes stretch this translates in to progressive pathology as the adipocytes are running out of their ability to function normally. As they get fatter they leak more FFAs at a given level of insulin. This is important. Very important.

Before we go on to the next post: Is there any other form of adipocyte insulin resistance, other than that due to fat distension?

I rather like physiological insulin resistance. It keeps me alive. Simple carbohydrate restriction or a couple of days of frank starvation produces whole body insulin resistance to spare glucose for brain use. You know what I mean. Take a young fit healthy human and starve him for three days and he will immediately become intensely insulin resistant on a whole body basis. If not he would become intensely dead. Are adipocytes part of this physiological insulin resistance response, in the same way as muscle cells are?

We get a partial answer to this when Hirsch cites Tucker's study and suggests that the reason she found no difference between the adipocytes of obese and slim rats was because both were maximally insulin resistant after a 20 hour fast, even those from skinny rats...

"However, these studies were performed upon tissue from animals fasted for 20 hr, a manipulation known to decrease the insulin response of adipose tissue in vitro."

Ad hoc number 3523, but highly plausible. Every body knows this... Physiological insulin resistance mimics pathological insulin resistance. The mechanism through FFAs is likely to be the same.

This would again be logical as you do not want rats in starvation hanging on to their adipocyte energy stores or to be allowing precious glucose in to adipocytes (however little glucose adipocytes use) and so allowing it to be "wasted" when needed by the brain.

Is there a third factor affecting adipocyte insulin sensitivity?

Well, of course adipocytes have mitochondria. Are they breakable? Probably.

If you break them I would assume that they behave much like those in muscle tissue and they do the best they can with pyruvate while leaving the FFA derivatives in the cytosol, ie adipocytes should become insulin resistant if they have broken mitochondria. But this insulin resistance is not stretch related and it's not physiological. It's a mitochondrial break and could happen at any stage of distension of adipocytes. So mitochondrial failure should lead to adipocytes leaking FFAs when glucose and insulin are elevated. Possibly at minimal distension size, ie while you are still slim.

This would worsen whatever state of insulin resistance the muscles were in from their own mitochondrial problems. If the pancreas is not up to overcoming the supplementary FFA-induced insulin resistance (due to its own mitochondrial problems as suggested by Petersen et al) then hyperglycaemia will result and you get that label of T2DM... Possibly while still slim.

The plateau in your weight here might be mistakenly attributed to the satiating effects of insulin on your brain finally kicking in, somewhat belatedly, after 50 years or so of hunger.

If you have an unbroken pancreas of steel you can still argue with the broken adipocyte mitochondria and you can still get even fatter. Ditto if you have T2DM due to insulin resistance and some joker gives you a bottle of injectable insulin plus some syringes. Especially if they also tell you to eat a ton of bagels and cover the hyperglycaemia with a ton of exogenous insulin. And chide you for overeating.

Peter

Summary: Adipocytes become fatter under the influence of insulin. Resistance to insulin by adipocytes limits fat storage and hence eventually limits weight gain. It also elevates FFA supply. Important.

96 comments:

So, in order to get to 400+ lbs, your adipose tissue has to retain some insulin sensitivity. Which I suppose has some genetic component. I made it past 350 lbs without getting full-blown diabetes, so I guess I was "lucky" in that regard.

Low-carb allowed me to lose over 100 lbs without excessive hunger. But since I am experiencing difficulty losing that last 50 lbs, I'm guessing that I have some mitochondrial damage (am I understanding all that correctly?). I go below 245, and all of a sudden, I'm hungry -- even on carb restriction.

I am currently doing the Fred-Hahn-style "slow burn" weight training, which I hope will help repair the mitochondrial damage and allow me to lose down to 200 lbs without being hungry all the damned time. I hope that works. Otherwise, I'm going to have to try something else -- or just die fat.

@ HowardI didn't have your challenge of losing so much weight, but I also couldn't drop my weight below certain level just by eating LC. In my case intermittent fasting helped. It really made the difference in dealing with being hungry.It was my New Year resolution to try IF. I found the website http://gettingstronger.org/2010/11/learning-to-fast/ to be particularly inspiring. As I understand, fasting is also beneficial for mitochondria. Just in case some worming - the more successful you are in the fasting, the more pronounced will be your physiological IR, especially after working out in a fasted state. I don't think it should a concern because it is reversible.

I'm still really concentrating on how mitochondrial failure fits in to the way I see metabolism working, so getting at practical solutions really will come from others with more experience of the practicalities.

Off blog Liz has sent me a whole load of links on hypothermia-stress induced protection against metabolic syndrome which fits well with the current line of thought and I will try to post about this "some day", as always.

These two clips were take at water temp 4degC, air temp was very low with a 20mph wind chill. We only get surf in the winter unless you are really, really lucky in the summer. I wasn't this year. I've never done this to breed mitochondria (though it probably does) but it's still a lot of fun.

I second the intermittent fasting plug. I lost 90 pounds with I.F. combined with C.R. In fact, I.F. makes C.R. a lot easier. I also found that macros and food toxins didn't matter to my weight loss at all. The initial loss was before I knew about "paleo". Plenty of Gatorade, burritos, cheeseburgers.....and exercise.

I've gotten the IF recommendation from a couple of other sources, as well, although the panel of experts on the last Low-Carb cruise didn't seem to think much of it. Also, the IF suggestions vary widely wrt amount and frequency.

Tom Naughton (the FatHead Movie guy) said he had some good results from staying in an 8-hour window, and avoiding eating the other 16 hours.

I guess I need to check around for some more specific IF recommendations to start with, and just try it.

I usually weight-train on an empty stomach, but I haven't tried it on a fast longer than about 6 hours.

You are using the term insulin resistance a little too loosely. The post is pointing out that adipocytes store fat under the influence of insulin. If they fail to do this they release FFAs inappropriately at a given level of insulin. They don't just dump all of their lipid stores.

If it is appropriate for adipocytes to release FFAs (physiological insulin resistance of starvation or LC eating), that's no problem.

If adipocytes are damaged and cannot respond correctly to insulin they equally inappropriately fail to retain fat even if insulin is high.

Had you specified pathological muscle insulin resistance in the presence of ample carbohydrate, rather than general insulin resistance, you end up with elevated insulin to get glucose in to muscles to maintain normoglycaemia. If adipocytes are still insulin sensitive they will grow under the influence of that hyperinsulinaemia untill they are as fat as they can get and become distension-induced insulin resistant at an obese size.

Note from Hirsch's work that the response appears to be linear, adipocytes do not have on/off switches for size induced insulin resistance, this feature is proportional and reversible when related to adipocyte size.

If adipocytes develop mitochondrial problems of their own they can become non functional before they become distended, so leak FFAs at inappropriate levels for the degree of hyperinsulinaemia.

LC works because all (non neural) tissues are meant to be insulin resistant in this state and what is pathological in the presence of glucose and hyperinsulinaemia simply mimics normality when glucose availabilty is severely curtained and insulin is low and only supposed to be minimally involved in energy supply.

I would not suggest that adipocyte insulin resistance shrinks fat cells during hyperinsulinaemic conditions but that it would stop them getting appropriately bigger.

The intersting question is what would happen if you specifically and suddenly targetted adipocyte (but not muscle cells) mitochondria with a toxin that only damaged adipocyte mitochondria. Fat storage would become impossible.

Rather like the autoimmune accquired lipodystrophes (which are propbably working at the whole adipocyte level) in which you become slim. Actually you become emaciated. And diabetic of course.

This blog should be required reading for anyone purporting to understand - or help - obese people.

It bothers me to no end that Guyenet keeps drawing the crowds, brainwashing dozens and hundreds, meanwhile he gets basic medical facts wrong and no one corrects or challenges him because he talks a good game.

@HowardThe very obese are usually not diabetic; that's why we aren't diabetic, because if you keep on growing new rolls of fat cells, due to insulin mediated adipocyte differentiation and enlargement, this clearly suggests that you do not have in place the conditions required for diabetes:

1) crap-out of fat tissue2) crap-out of pancreas

If either of these crap out, it's dialysis for you.

To find out what happens when the fat tissue quits this b*tch, google "lipodystrophy diabetes" and just take a look at that clinical picture.

NO need to google pancreatic crap-out, as it is beyond obvious that insufficient insulin will cause diabetes. This was the first form of diabetes discovered: the rapidly fatal type 1 form.

What is lesser known is that adipocyte crap out also very swiftly brings on diabetes, and in the type 2 form, it is safe to say that in a lot of cases what you are observing is adipocyte crap out (severe resistance). These people can no longer grow, or expand, their fat tissue to cope with their metabolic disorder, and so it is almost as if they have no fat tissue at all (go back to lipodystrophy to reference what happens there).

If you keep on getting fatter and more obese, your glucose tolerance tests are going to be very good compared to a much thinner, chubby, all belly type 2 diabetic who spikes to 350 after eating pasta.

The reason you become hungry below 245, is probably because of adipocyte hypotrophy. Your fat cells, at this weight, may be "normal" sized, and refuse to easily release more fat without a fight.

High insulin doesn't just makes fat cells expand in size, it makes them increase in number. That is permanent, like a tumor is permanent. You are permanently overweight after morbid obesity, and the only work around that is medical:1) inject leptin (mimic normal fat tissue/normal fat cell size) and/or 2) use a surgeon's catheter to instantly suck up the abnormally hyperplastic fat tissue, thus normalizing endocrine dynamics with the fat tissue.

I've had 30,000 in fat cell removal/skin removal and it is SO MUCH easier to maintain my weight now, at this size, than it was before the surgeries. I look less starved even though my weight is the same (hi cheeks which are not all bones). I've had a lot of weight in pure skin removed; my fat cell #s are probably still significantly higher than a non-obese person, but they are much more normal than they were before having several kgs of deflated fat cells surgically removed.

I know it sounds like some crap a sandal wearing vegan might promote, but I SWEARZ since drinking this like water it seems to be targeted every core problem I have run into after losing weight/lower leptin post weight loss.

-GT leads to an increase in lean mass as well as a loss of body fat (this is similar to leptin normalization post weight loss, and increase in IGF1/decrease in IGFBP)

-My mood is higher/my blink rate is higher (signs of higher dopamine; EGCG/GT inhibit COMT, and dopamine is a major metabolic controller FYI mediating starvation adaptation, hibernation, as well as pathological obesity... blink rate increases or decreases reliably predict CNS dopamine). This is similar to how leptin is a necessary hormonal prereq. to have normal dopamine synthesis, storage, and release to daily events.

-It is an alpha-5-aromatase inhibitor, which lowers DHT and increases testosterone/estrogen; this further helps mood and glucose tolerance as I have estrogen insufficiency from leptin insufficiency, and lowering DHT/raising estrogen makes skin nicey nice.

As retarded as it is, drinking heaps of green tea has been one of the most theraputic, non medicinal weight maintenance interventions I have found which helps to correct every single aspect of weight loss difficulties.

The funny thing is I always knew even small doses of green tea made me feel "better" and made my skin "nicer", but I ignored this because like, duh, supplements don't work we are all told.

Since I am always right about everything, and my track record of not being wrong is pretty excellent, I decided to just drink a lot of green tea. Since doing so I have benefited immensely. I literally feel almost the way I did while taking leptin.

No, obviously not that effortless, but it did help a lot.

I mean, get some strong green tea, brew it, chill it, put splenda in it, and drink a litre of that. You will feel warm, your mood will increase, you will tolerate carbohydrate better, you will have appetite reduction and an increase in energy.

Part of me suspects most of the benefit is in dopamine augmentation from green tea/inhibition of COMT. I have consistently observed my whole physiology depends on my dopamine status, even while on leptin replacement. If I am blinking a lot, it's good times all around, in every aspect of physical and emotional wellness.

Which is why I have come to believe many forms of obesity are a form of seasonal adaptation, controlled by dopamine, triggered by carbohydrate, which is otherwise seasonal.

I think Peter is right about insulin and obesity, and Stephan is wrong. The missing link in this debate is magnesium deficiency, and it's strange that Stephan has not made this connection because he's written some excellent posts about magnesium.

Obese people have been found in several studies to have a low magnesium intake, and low blood magnesium is characteristic of insulin resistance.

'Intracellular calcium plays a key role in metabolic derangements associated with obesity. .. increasing [Ca2+]i appears to promote triglyceride accumulation in adipocytes by exerting a coordinated control over lipogenesis and lipolysis, serving to simultaneously stimulate the former and suppress the latter, resulting in lipid filling and adipocyte hypertrophy.' ('Role of intracellular calcium in human adipocyte differentiation', 2000)

So the question is whether insulin increases adipocyte calcium. See 'Chelation of intracellular calcium blocks insulin action in the adipocyte' (1987).

However in human obesity, adipocytes already have a lot of calcium, and insulin doesn't increase it very much. See 'Possible role of cytosolic free calcium concentrations in mediating insulin resistance of obesity and hyperinsulinemia' (1988).

But insulin does increase it, and obese people have a lot of insulin. So it might work.

Why do they have a lot of insulin? Well, insulin is supposed to inhibit its own secretion, and this is mediated by PI3 kinase, which requires magnesium. ('Insulin receptor activation inhibits insulin secretion from human islets of Langerhans', 2001). So hyperinsulinemia in obesity might be due at least in part to magnesium deficiency.

So what about insulin and the brain. It's supposed to be 'satiating', ie it makes you thin, not fat. Downstream of insulin (and leptin) in the brain is once again, PI3 kinase. Without magnesium, insulin might not be satiating.

In fact it's well known that magnesium deficiency leads to sugar cravings, and magnesium increases brain dopamine. Perhaps the elusive 'food reward' is actually magnesium. You don't stop eating until you have enough of it.

Maybe this is why low-carb diets work: they eliminate carbs which have had their magnesium removed. Without magnesium, carbohydrate is useless as a fuel, and will end up as fat or as reactive oxygen species.

BTW, that bland liquid diet (Renutryl) that Stephan told us causes weight loss despite being full of refined carbs, including sugar, also contains magnesium.

Appreciated your response to Chris--a clear summary of your post.Enjoyed the wave riding video-what an exhilarating sport. In Montana where I live, I am all downed up in January when I go backcountry skiing. Would it help my mitochondria if I wore a shorts and a t-shirt? What do you wear in such cold conditions when you are out on the waves-a dry suit?

ItsTheWooo2:

Whenever I try to read Stephan's posts I have a hard time trying to understand what he is communicating. I don't know if I am the problem, or if he doesn't define terms and concepts or has logical or conceptual gaps in his arguments? I can't make sense of what he is saying. I know if I posted this on his blog, someone would probably berate me for being stupid.

Is it really true that the number of fat cells cannot be decreased except by surgery? I hear that a lot, but it strikes me as a bit odd--the body is so good at getting rid of other things it doesn't need...

@Anon any bitter tasting (the bitter is the good shtuff!) green tea will work. I used trader joes brand. I have observed an effect even from bottled lipton diet green tea, which contains only a fraction of the egcg/catechins of fresh brewed green tealeaf.

I appear extremely sensitive to the benefits of GT and as I said, I believe most of the benefit is in COMT inhibition, with a secondary benefit being estrogen augmentation, as I have consistently observed my whole entire metabolism and outlook depend on these variables. COMT inhibition leads to higher CNS dopamine. There is oodles of research out there about how dopamine completely programs the metabolism, and much weight loss adaptation is mediated via low leptin leading to low basal dopamine stores. Anything that can correct that, will make you naturally thin. Normal dopamine signalling = naturally thin with good glucose tolerance, or at least it is an absolute prerequisite.

I am absolutely positively sure it is not placebo - to test my idea last night I brewed very strong GT and drank several cups circa midnight. By 3 am I was HIGH AS A KITE, I mean, it was like amphetamines. I was blinking, laughing, hyperactive, euphoric, music sounded fabulous, I was warm and flushed, these are clearly dopamine/norepinephrine mediated effects.

I am also taking amino acids that augment catecholamines, so I suspect there is an interaction.

Either way, it is beyond evident to me at this point in time that the substances in GT are highly valuable for people attempting to maintain a reduced weight, as they seem to specifically augment dopamine , and that is where everything depends. Dopamine is how leptin works.

@DavidLike beth said, leptin mediates adipocyte apotosis; however, the trick is, leptin reduction is part and parcel of successful weight loss. Tricky. Leptin declining after starvation (the only natural evolved reason for leptin to decline) helps the body defend against future famines by permanently raising body fatness.This is the reason behind the common observation that after a crash diet (which, to our physiology, is nothing but starvatio) people are permanently fatter.

Think about it: why would the body have a system in place to terminate excessive fat cells? To assume this is in place, assumes that obesity is natural and normal, when clearly it is not, obesity is a modern environment side effect of chronic hyperinsulinemia.

Assuming that the body will one day kill off all the extra fat cells it grew from hyperinsulinemia, is like assuming that tumor on your forehead will magically fall off one day because after all the body doesn't need those extra skin cells.

You may know that, but the physiology running your ship doesn't know that. All it knows is fat cells exist -> maintain size of the fat cell via leptin signals at varying intensities, controlled by fat cell size and energy balance up or down. WHen the fat cells reach a small size, the leptin signal drops off, and your WHOLE BODY is like "EAT YOU DUMB ASS, AND STORE FAT".

There is no 'lets get rid of our fat cells for some perverse reason" program in place, because obesity : insulin mediated adipocyte hyperplasia - is totally evolutionarily impossible as far as our GENES are concerned. Being a 500 pound ball of fat is just not something we ever evolved to encounter, this is purely a modern side effect of drinking corn starch 24/7. From an evolutionary perspective, terminating fat tissue is absolute madness.

@ AnonI personalty found a loose-leaf Jasmine tea which is sold in Oriental stores to be quite palatable. I also put a slice of lemon into it.It helps me to switch off impulses to eat something that it better to pass.

Rodents are not perfect models of human disease or metabolism, but to say that we can learn nothing from them is, to say the least, a bit silly.

A great deal of our understanding of apoptosis comes from studying a microscopic worm, Caenorhaditis elegans. Almost all of our understanding of mitochondria and the Krebs cycle comes from non-human organisms.

While any study using an animal model of a human disorder needs to be examined carefully before jumping to conclusions, when someone discovers a basic biochemical relationship in another species, it is worth taking into account, isn't it?

"I can't make sense of what he is saying. I know if I posted this on his blog, someone would probably berate me for being stupid."

When one starts with a conclusion and works backwards, it is often necessary to skip over, gloss, conflate, or otherwise befuddle the explanations of the parts that don't support the predetermined endpoint.

If you haven't seen it already, I invite you to read my ongoing series Why Are We Hungry?, to ask clarifying questions if necessary, and to compare your befuddlement before and after doing so.

When I studied food science at university over 20 years ago I was taught that you can't even legitimately extrapolate dietary studies across different ethnic groups. If I swapped diets with an Okinawan both of us would probably be in hopital within a week. I can't tolerate carbohydrates or fibre and Okinawans can't tolerate large amounts of dairy food.

Dietary studies are totally species specific. They are not molecular biology studies trying to determine basic biochemical mechanism shared by all animal species.

Rodents have arguably the least human-like digestive system of any non-ruminant mammal. Rodents convert most of their carbohdrates to SCFA and amino acids in the cecum. Humans absorb most our carbohydrates directly from the small instestine.

The natural diet of rats and mice is primarily seed based and typically contains about 80-85% carbohydrate (starches), 10-15% protein ands <5% fat. Rodents also require an extremely high fibre content. No human society eats a diet anywhere near as low in fat or as high in fibre as a rat or mouse.

@WoooThe reason green tea makes you feel so good is probably because it corrects iron-manganese imbalance. It is extremely high in manganese, and has been found to prevent iron absorption.

Iron-manganese imbalance is expected from a high intake of red meat.

It sounds to me as if you have some dopamine malfunction. This would be consistent with iron-manganese imbalance, because manganese protects the dopamine system from iron-mediated damage, see this paper:

http://www.ncbi.nlm.nih.gov/pubmed/9681949

You told us you do eat a lot of red meat, partly because people who do not eat meat are religious nuts, and partly because it prevents anaemia. Did you know that anaemia often co-exists with iron overload? I suspect your anaemia was/is caused by copper deficiency. I know you think you have copper overload, not deficiency, and I think you are wrong.

Diagnosing copper deficiency is so difficult that by the time it does get diagnosed, it's usually too late, and the damage is permanent. Watch out, Wooo.

This is much in the way gasoline, oily rags, and a spark of fire are not mutually exclusive components of a horrible devistating fire that destroys your home.The fire could not have happened if either of these components were not in place. You can't burn down a home without a spark, and you can't get a nice blaze going without energy from oily rags. Remove one of these, reduce one of these, the fire is better, or never occurs.

This is like carbs and calories for many if not most forms of obesity.

This is such an understated point. Even between human ETHNICITIES, there are wide leaps in what one genetic group can or can not tolerate, or thrive on. HUGE.

We also see a in medicine where diagnostic tests, and drug therapies must be tailored to the ethnic group; this is not widely discussed/taught as it is not politically correct to admit there are differences between human groups, and the result is patients suffer from physician ignorance (just add a little heap more to the big giant pile of existent ignorance, I suppose).

The very core foundation of a cell level function is quite a different thing than the complexity of an organism and its functioning. It would be like saying; the pigment blue is on a stripe on the side of a plane, and it is also the color of a child's ball; therefore, these objects have relation and must function in a similar way. If two objects share a similar base element(s), it does NOT mean those elements combine in the same way to create similar function.

Jane - I respectfully disagree. I know you love minerals, but the benefit is clearly from the catechins, which do numerous things other than alter manganese (even if they are doing this). I wrote a long blog post about it.

As stated I believe most of the benefit is COMT inhibition as the way it makes me feel is pretty specific for dopamine-y good times. I blink more, I want to move more, I feel optimistic and even elated, music sounds wonderful, my appetite is quite low and my glucose tolerance is awesomeness and I have tons of energiez. I have long observed myself with my energy and mood states and I am quite familiar with the signs and symptoms of higher CNS dopamine, and those be DEM. The signature is the elevated blink rate + spontaneous facial gestures.

The way it works is that catechins get caught up in the COMT (perhaps this is because of of their molecular structure, hense their name). The end result is the COMT you are generating is not acting quite as much on dopamine/norepinephrine as it ordinarily would, because it is flubbing up dealing with the catechins you done DRANK UP in your green tea! Brilliance. The effect is even more augmented if you down up some tyrosine along with your catechins.

Like I said, midnight, I drank 3 cups of strong green tea. Caffeine content a pathetic 90mg acording to the interweb, but OH MY GOD I was high as a kite until 3 am. I have not had energy like that in months.

There is no way 90mg of caffeine alone could make me feel that way. Trust me, I am very familiar with caffeine stimulant effects, and for someone with my tolerance 90mg is like, pppppshhh next plz.

I find it very hard to believe this is manganese, I am taking a manganese supplement for a few wks and I never noticed anything close to that.

FYI I also notice I feel better when I take more copper (I dont care about RDVs, even though I drink mixed nuts like water so my RDV for copper is like 400%, I still am taking more supplemental copper - I also think this is helping since I have always noticed better moods when I take more copper and I think copper + magnesium is important too). So, FYI, my copper levels are probably quite high. I eat a lot of meat, but I also eat a LOOOOT of nuts. I don't eat red meat that often, not by choice, merely because I am too lazy to cook more often.

Dr B was a heavy influence on me when I was just a beginner at LC. The man has a lot of experience. His forum is excellent (no time to go there now). I would be the first to admit that my adherence is no where near as close to the OD as a a full blown diabetic needs to be to Bernstein's approach. But I am gifted with a fairly functional pancreas, as far as I can tell...

Although your clearly just being sarcastic and think this is all some kind of joke, you MAY gain some self respect if you actually tried your 4000 calorie fat only experiment.

Not only that, youd be surprised at the results.

lipid consumed in isolation has very limited palatability, consumed in isolation it also sends GLP-1 through the roof, this would keep you extremely sated. To reach your 4000 calorie target you would have to endure the extreme discomfort that comes from forcing food down your throat when you have the completely gorged feeling.

You should really try 5000Kcal a day of mostly fat, really. You will then maybe understand that it's nearly impossible to sustain that long enough to get fat. You will be so nauseated that the idea of even eating will send you to the loo. That's the magic of metabolic advantage, you won't be able to eat that much fat. 5000 kcal of fat is half a liter of oil, it's more than 1kg of cheese or around 1kg of bacon.Add some carbs and it gets easy to eat that much on 1 day.

I'd also like to point out, in Stephan's blog, those rats that were fattened with their 'high-reward' diet, when they returned back to the normal 'low calorie' diet, they did not lose ALL the excess fat they gained, meaning the body set point seems to have actually shifted to make them more fat.

Stephan doesn't dwell on this point, but just mentions it in passing, but it seems to be very significant, which is quite simply, it isn't all about calories...

Rodent studies are consistent with those in humans. Returning rodents made obese using palatable high-fat diets or chocolate Ensure (or by gavage overfeeding) to ad libitum ordinary rodent chow makes them lose most of the excess fat, although some of it is often retained (16, 17, 18).

Its funny you mention lyle mcdonald, in one of his books he mentions how something like 6000 calories is needed to gain weight on a ketogenic diet. He also mentions how insulin and glycogen are important rate limiting steps for ketogenesis, without them, ketogenesis proceeds at its maximal possible rate, determined by FFA availability,

its why type 1 diabetics are at danger of ketoacidosis, without insulin, ketogenesis proceeds at a very accelerated rate.

Peter and Itsthewooo,I have a few ideas that have been stirring and wonder if you guys could help me out.

First is Wooo.Just today it hit me that mon,tue and wed I have been drinking a half gallon of Splenda sweetened Green tea and find that it definitely helps me to lose weight and feel much better.Thur,fri and then sat and I backtrack and get all bloated out and start gaining fat.I can't believe to see you experiencing the same thing and posting it here(freaky).So today I was wondering if its the slight caffeine boosting the metabolism but you write its the catechins.I remember reading awhile back some scientist saying that if your metabolism is destroyed then that could mean a lifetime of thyroid meds and ephedrine to spark the system.So I now wonder will the benefit of green tea eventually stop working when the body adapts?

Peter,I have been wondering about a reason for LC diet to fight against obesity.Could Steatorrhea actually be the bodies mechanism to prevent obesity.Steatorrhea is looked at as bad since it means you are not absorbing nutrients instead pooping out the fat.Couldn't this be natures way of acomplishing two things.

First is the prevention of obesity.....you just can't absorb enough fat to get super obese if your bile production is impaired.

Second is prevention of constipation.

I ask this because a few weeks now I have been experiencing Steatorrhea and was worrying at first.But now I wonder if I should be worried.See I had constipation for 3 days....that rock hard gut feel that too drastic a fat reduction causes.So I added in 1200cal in butter and the next day I was sitting on the loo all day.I had the tell-tale Steatorrhea very pale looking stools that would stick to the side of the toilet.I guess I just want opinion Peter on this idea?

Thank you for the link to your website. Hopefully your website will help me understand Stephan's arguments? I am not comfortable asking for explanations on his blog because of the level of hostility I have noticed in some of the comments when there is a difference of opinion or a lack of understanding. As I stated, my lack of understanding of Stephan's food reward theory may just be my problem.

Cwaiand - Few people argue calories do not matter.We are arguing that carbohydrate - the primary catalyst for hyperinsulinemia/being hugely fat - is what matters most. When you get that handled, then it becomes even POSSIBLE to contemplate energy restriction (and have a shot of long term success).

Hey, here's a 411/FYI!I'm a 5'5 female and my high weight was a massively obese 280 lbs. The only reasont his was my high weight, is because this was as fat as I got until I discovered low carbing. Within hours of finding out this existed, I stopped gaining weight and began rapidly, uncontrollably LOSING weight, purely because my entire endocrine system normalized within hours of starting this diet. If I did not, at that time, accidentally discover low carbing, I have little doubt I would be over 300 pounds today, among other problems.

That was almost 10 yeras ago and now I am 117 pounds (according to the scale 2 days ago) and I have never been even close to overweight since.

I don't exercise at all. I don't eat a "low reward" diet, I love yummy food and eat whatever tastes wonderful.I do not starve myself (although I do watch calorie intake, I never go hungry, and the only times I do restrict calories significantly, it is done in an attempt to fix my blood sugar which was previously screwed up from eating carbs).

I mean, I pretty much do nothing to stay this slim, other than focus all efforts on blood glucose & insulin suppression (supplements/lifestyle/food choices).

This just does not happen by accident. I am able to do this because my choices are informed by reason, personal observation, and science.

Sorry you are under the delusion that you are getting fat on a very low carb/high fat diet (fact: I dont believe you at all, unless you have a rare form of obesity unrelated to glucose intolerance/hyperinsulinemia).

As long as you remain deluded that this thing called "calories" are driving you to pathologically and abnormally store fat with no ability to self regulate body weight, you will continue to struggle as much as you do. "Calories" are not what is driving your fat tissue to expand uncontrollably with symptomatic hyperphagia. "Reward" is not either. That thing is insulin, assuming you are otherwise genetically normal/genetically "gifted" In fat gain potential.

@ cwaiand It looks like your got your mind set by now, but I decided to try anyway, may be because it is rain and nothing urgent to do right now. I am one of those who lost weight on a LC diet. I was sort of chubby all my life, never obese, going on and of diets, an exerciser, not a junk-food consumer. I was not thin because somehow I was very hungry too much too often Then at 45 all diets stopped working, chain of sport injuries happened,weight gain of 26 lb (BMI got around 31) followed, cluster of health issues...My doctor told me I was just getting older like everybody else.Finally , at 46 years old LC killed my hunger. Now I can do cardio just 3 times a week instead on 1.5 hour every day. Call me lazy, but I am just feel free now. I eat only two times a day a high fat food and veggies. I think many people who can't loose weight on LC eat by high-carb pattern - 3 meals a day + at least 2 snacks, or just manage to find versions of LC foods they can eat compulsively.For many it is cheese.For me it would be nuts, that is why I don't keep it at home. I can't contribute to the discussion about calories because I never count it, only make sure I eat to satiety each time when I eat. At the beginning of April I clocked at doctor's office the loss of 30 lb, it is 35 lb now. Not a lot for almost 4 years but it was my goal weight and I intend to enter my information into National Weight Registry in about 6 months. My doctor was amazed, he told me it was against data in medical literature that somebody could not regain weight after loosing some. I doubt my story would be so successful if I decided to drink some tasteless substance through the straw for 4 years.

cwaiand It looks like your got your mind set by now, but I decided to try anyway, may be because it is rain and nothing urgent to do right now. I am one of those who lost weight on a LC diet. I was sort of chubby all my life, never obese, going on and of diets, an exerciser, not a junk-food consumer. I was not thin because somehow I was very hungry too much too often Then at 45 all diets stopped working, chain of sport injuries happened,weight gain of 26 lb (BMI got around 31) followed, cluster of health issues...My doctor told me I was just getting older like everybody else.Finally , at 46 years old LC killed my hunger. Now I can do cardio just 3 times a week instead on 1.5 hour every day. Call me lazy, but I am just feel free now. I eat only two times a day a high fat food and veggies. I think many people who can't loose weight on LC eat by high-carb pattern - 3 meals a day + at least 2 snacks, or just manage to find versions of LC foods they can eat compulsively.For many it is cheese.For me it would be nuts, that is why I don't keep it at home. I can't contribute to the discussion about calories because I never count it, only make sure I eat to satiety each time when I eat. At the beginning of April I clocked at doctor's office the loss of 30 lb, it is 35 lb now. Not a lot for almost 4 years but it was my goal weight and I intend to enter my information into National Weight Registry in about 6 months. My doctor was amazed, he told me it was against data in medical literature that somebody could not regain weight after loosing some. I doubt my story would be so successful if I decided to drink some tasteless substance through the straw for 4 years.

i knew everyone would rip on me not being sucessful on high carb weight loss.so i lied.i,m currently 190lbs at 6'1" tall.my high weight was 320lbs(all fat).i lost and maintained my current weight for the last 7 years.how?eat less move more.

i became a bodybuilder.lift weights ,follow a calorie restricted fairly low fat average protein and 50% carb diet.now i,m sure you must realize that can,t have happened seeing as i ate carbs.

it,s the wooo,you didn,t lose weight before low carb because you were lazy and over ate .

please go help jimmy moore,he,s sooo sucessful on low carb.when he stops loseing weight the advice given him was "not enough fat".now he adds 12 tables spoons of butter to his huge steak.his weight then goes up higher.hmm i guess not enough added fat.

you folks are really starting to cause alot of harm.

soon though enough failed low carbers will surface and this charade of dis-information will come to an end.

My weight loss was very-very slow. Some of reasons for that are probably pre-menopausal age, under-active thyroid, long history of dieting. I know from experience how to loose weight by starving myself while exercising, I did it many times,I would continue doing so if it would worked after 45 yo because I knew the drill. My hunger disappeared the day I started LC, leg edema gradually diminished during first 3 days, energy level improved really quickly. I have never ever had an abnormal blood pressure.During summer I put my 75 yo mother(and 4 more ladies) on LC - her blood pressure became normal during first week, hunger disappeared . She lost only 23 lb and weight loss stopped.

your low thyriod maybe caused or made worse by very low carb eating.i,m of the mind that, seeing as your brain requires around 150 grams of carbs a day ,you may as well eat that much.why convert protein for the brains glucose requirement?

so 150 gram carb around 100 gram protein and the rest fat up to calorie requirement.these numbers would be for a sedentary person.work out and your protien needs go up some and of course your carb requirement goes up even more so.

it,s the wooo;it seams to me you have a poor relationship with food.i mean if you need to have a relationship with food i think there is a problem.your now looking for the next "magic "food substance.green tea is the flavour of the month.i would like to see any scientific papers supporting anything green tea. anicdotal,ya sure tons out there.real studies ,controlled scientific,i don,t know?

This really isn't like me at all, oh my I am in a diplomatic mood, but I am going to completely ignore this obvious troll. Yes, professor - nay, PRESIDENT of wt loss infoz, you have clarity and vision and foresight to know that one day, I leapt up from my chair and said ENOUGH1!!111 i WILL NO LONGER BE A FATSO AND i WILL MAGIALLY MAKE MYSELF ENERGETIC AND NOT HUNGREE!"

After I made that decision, I just you know stopped being fat and lazy and choosing to eat a lot of food, choosing to be so tired and apathetic I could hardly move. I just blinked and cured my brain like charlie sheen did.

Here we have a case study of "Typical bodybuilder". He's got the 'tude and ridiculous obsession with judging people based on their body and weight and eating, CLEARLY bloated with psych neurosis to compensate for the body fat % he has whittled down via cutting and muscle hypertrophy. Ironic he accuses me of having psychological food problems, when he's the one sitting in a gym lifting heavy objects all day for no reason, all so he feels superior and better and full of WILLPOWERZ that fat slobs do not have.

I also do not believe you were ever 320 pounds. Anyone who has lost and maintained as much weigh as you claimed to have KNOWS it is not as easy as making a "choice" to just stop being hungry and stop feeling tired.

i don,t have low body fat.maybe 12%i,m not a competitive bodybuilder.i used weight training to get i nshape and help lose weight(also a great way to control appetite).i spend maybe 3 hours a week on weights and i go for about 5 hours of total walk time per week.combine that with a proper(includes carbs)calorie resticted diet and your all set.i did peak at 320lbs and have been at 190 for 7 years steady now.

you say i magically desided to not be hungry and move more.that is how it,s done.

do you not see that your weight loss journey was all about decisions YOU MADE?you took steps that helped you to cut calories.that,s all that happened,no magic,YOU DECIDED TO FINALLY GET A HOLD OF YOUR WEIGHT.

YOU WANT IT TO BE SOME MAGIC like insulin locked my fat in so it could not be released.not how it works.you finally made a decision to no longer be fat and stunbled onto a type of eating that helped you to CUT CALORIES.

oh and as far as being tired and lazy,i had that too,big time.it,s called being fat.lose weight energy comes back.

this shit is really not that hard.too many people reading about weight loss and not acting on weight loss.

O.k., it is another day, no more rain, just some clarifications and I am over. My thyroid condition was diagnosed more than 15 years ago, autoimmune in origin, didn't get worse after LC diet. In some way I am a special case because I started VLC in order to control migraines and it worked. Brain functions very well om ketones.I have to admit - I am too lazy to micromanage my diet, count calories, and life time of dieting made me tired of being hungry. It is very convenient that just eating high-fat-normal-protein diet allows me to eat enough in order to be full and manage my weight at the same time. Actually all my adult life I looked around and thought-"Why other people could eat and stay at good weight while I am at constant straggle not to eat and exercising too much?". My straggle is over because now I can eat till I am full if I avoid carbs. I agree that 150 gramm of carbohydrate are not excessive for human metabolism in theory, but for people with tendency to gain weight such amount makes all the difference in our ability to control our weight and health. We suppose to listen to our body, right?. I tried different diets, LC is the only way of eating you can eat forever and not develop an enormous desire to pig-out eventually, unlike cabbage soup, plain potatoes, tasteless fluid. If you can eat forever like Bill Clinton, or there is no difference for you between McDugal diet and High-Fat diet - then follow either or just give-up. Unlike you, I am healthier than 4 years ago and at the desired weight.Sorry, Peter, I will not clatter your space any more.

you are talking nonsense. The scientific literature clearly shows that calorie restriction and exercise have a less than 1% success rate after five years.

Hundreds of millions of overweight people can't all be stupid lazy gluttons.

as far as the last comment goes.

uhh never said stupid .lazy yes.we setup our society that way.laziness and over consumption.

ever met a obese person who didn,t over consume junk food?not likely.nation of people in denial looking for an easy out instead of standing up and taking control.

unemployed peolpe are unemployed by accident>?ya like rich people get rich by accident.

obese people are obese because they choose to be.i do think it is mostly a phycological problem based on self image and depression.

i used to buy into the"it,s not my fault i over eat"like my mind had no control over mindless eating,you know what?it,s just that,mindless eating.use your brain that,s what it,s for.people want to compare us to other animals or primitive humans when it comes to obesity,guess what ,we,re niether of those.

OWN UP,USE YOUR BRAIN,GET OFF YOUR BUTT AND STEP AWAY FROM THE COMPUTER.

they tell me to eat 4000 calories of fat and in the abcense of carbs i won,t gain fat.what a joke.energy excess doesn,t count."

Huh? You got posters telling you on here it isn't possible to eat 4,000 calories of fat, because you would get nauseous... Why do you think most LC dieters argue that fat must NOT be accompanied by calories from carbohydrates, if it wasn't about energy excess?

they tell me to eat 4000 calories of fat and in the abcense of carbs i won,t gain fat.what a joke.energy excess doesn,t count."

Huh? You got posters telling you on here it isn't possible to eat 4,000 calories of fat, because you would get nauseous... Why do you think most LC dieters argue that fat must NOT be accompanied by calories from carbohydrates, if it wasn't about energy excess?

asim;

seriously,your talking in circles here.

you say i can,t eat 4000 calories a day of fat,"i will get nauseous".in other words it,s all about the calories .your saying i can,y physically eat 4000 calories so the calorie restriction is what works.ok so i agree CALORIE RESTRICTION WORKS.

then you suddenly throw carbs back in to the equation.so i f i add in say 300 grams of carbs,now i can magically consume 4000 calories of fat and not get naseous.do you see how rediculous this is ?i mean really.

ok so i,ll down pure coconut oil and butter sticks.shpould be no problem to get to even 6000 calories a day.i,ll add in 50 grams of protien so i don,t waste away.NO CARBS.then i can sit back and watch my weight remain stable.

man some folks on here are completely lost.

peter should set you guys straight,he doesn,t speak of such bullshit ideas as some on here do.

You obviously missed the point, which is you are claiming that people on this forum don't believe in energy excess, because they suscribe to a low-carb diet. The two are clearly not mutually exclusive.

One LC person on this forum made it clear that it is pretty much impossible to eat 4000 calories of fat, meaning it's ability to cause satiety is one of the reasons for it's success. When one is satiated, one eats less calories.

Other people argue that cutting calories works, but certain types of food such as many starches, causes rapid rises in insulin to handle the rapidly rising blood sugar levels. When these levels drop, this lead to a huge increase hunger, which may cause one to over-eat, i.e. again energy excess. Fat, on the other hand, maintains steady insulin levels and the issue of hunger does not come as much into play, meaning less energy consumed in the long run.

These examples all strike directly at your claim that LC dieters don't believe in energy excess.

"then you suddenly throw carbs back in to the equation.so i f i add in say 300 grams of carbs,now i can magically consume 4000 calories of fat and not get naseous.do you see how rediculous this is ?i mean really."

Yes, I agree this conclusion is ridiculous, which has nothing to do with what I stated.

The point is, if one suscribes to LC, one may say the insulin rise associated with carbs causes a rapid influx of 'calories' into the cell, not allowing the mitochondria to properly handle this energy load, meaning energy excess is still in the equation. Without the insulin spike, the calories are handled differently.

"then you suddenly throw carbs back in to the equation.so i f i add in say 300 grams of carbs,now i can magically consume 4000 calories of fat and not get naseous.do you see how rediculous this is ?i mean really."

This is not as far fetched as it may seem. see the study I link below.

Fats ingested alone = big GLP-1 spike,

Fats ingested with carbs = no GLP-1.

ooppss..

One of the reasons Roux-en-Y patients cant stuff thier faces with calories is because they are hypersecreting GLP-1.

Dr. Ayers, without getting into the details, believes that in a high-fat diet, with very minimal carbs, is that excess fat (energy) leaves via cytomembranes, through HDL, into the bile and out your poop.

Whether this opinion is correct or not, it clearly establishes the point that the LC arguments are normally about energy excess, but in the context of how that extra energy is handled when one adopts this sort of diet.

@BlogBlog,it could very well be that it goes away after a week and gut flora based.I binge on wheat stuff like beer and pizza every weekend and can tell you the amount of yeast I shit out for the first two days going back to LC is amazing.

I have eaten 1000calories today and if it was with alot of carbs I would explode with hunger right now.Since I ate LCHF today I feel my hunger is manageable.This is due to my hunger being REAL hunger and not my brain sending signals to eat to bring back up the blood sugar.

Asim,pooping out excess fat calories is very reasonable idea.Afterall,we all have varying amounts of bile we can produce per day.Could explain why some people can go to 4k to 5k and not gain fat.I mean are we really to believe that the metabolism speeds up to burn an extra 3k calories just because we keep carbs low?

I'm glad someone else can verify this substance seems to be theraputic for obesity. I realize it sounds crazy and like it shouldn't have any effect, but I cannot argue with what I am seeing, it does feel vaguely like I am taking leptin again. I had pinned down that most of leptin's benefit is downstream of dopamine (leptin is required for normal dopamine, and dopamine then completely controls EVERY ASPECT of metabolism mood appetite and energy). GT seems extremely valuable for augmenting dopamine, at least in my body. I cannot state everyone will react this strongly.

It's definitely not the caffeine. I am well familiar with what caffeine does. Caffeine can NOT do this. There is probably a synnergy between GT and caffeine (research supports this; catechins alone are not as effective as catechins + caffeine, presumably because catechins work by blocking the destruction of dopamine, and caffeine also raises dopamine. Fortunately GT contains 30mg of GT per 8oz serving so natural source of catechins - gt - also comes with caffeine.)

Regarding your fear it may stop working... I don't know. I have been using it for a few weeks now, on accident, and I have not noticed a return to the shit(tier) state I was in before taking lots of green tea. I have not noticed any weakening in potency, my brain so far has not adapted significantly. It stands to reason that the brain will eventually adapt by downregulating dopamine receptors, but I'll be posting regularly on my blog if you are curious. This is all hypothetical, there is HEAPS of research supporting the glucose tolerance/mood/body fat/lean mass improvements from GT, but I have not seen any research group try to actually aplpy this substance to weight loss maintenance groups (I think weight loss maintenance groups or active dieters would be the ones to benefit the MOST from GT, as we are dealing with leptin and subsequent dopamine insufficiency).

It's the end of the day and I barely ate any food... yesterday I ate 1000 calories. Prior to taking green tea this would ahve been IMPOSSIBLE. My energy is quite good and my blink rate is higher, which is specific for dopamine. I am not cold. I can eat carbs, within reason, and not experience quite as much abnormal hyperinsulinemia (as it was on leptin). My energy remains in tact after eating a meal with carbs, or at least it is much less of a problem than it was before the GT.

The only reason I am not losing heaps of weight is because of my nursing job I work 32 hrs in 48, which requires extreme sleep loss for 3 days straight. That jag of not sleeping is what is keeping my weight stable. When I do not sleep for that amount of time I begin eating a lot of food and my blood sugar/insulin just goes to hell. But if I was NOT working in this manner, or alternatively if i used WILLPOWERZ (nod cwaind) to starve myself during the high insulin insomnia jag, I would surely be losing weight.

I have no period of fasting during my "working marathon", and I think fasting , even if during sleep, is crucial for not being a fatass. Insulin remains chronically elevated when you are eating at 3pm, eating at 6pm, eating at 11pm, eating at 3 am, eating at 8am, eating at 12pm. You sorta eat like that when you stop sleeping. Your blood sugar control becomes non-existant when you are awake that long. Crushing hypoglycemia under trivial durress that you could easily tolerate while rested normally.

Another great thing about GT is that it strongly suppresses my caffeine cravings. Prior to using GT I had overwhelming cravings for caffeine and stimulant effects of it. I think this is more evidence that GT is correcting a dopamine insufficency (secondary to leptin insufficiency). Some days I barely take any caffeine now that I use GT and I feel fine; in the past this would have been impossible. There is no way I am drinking as much caffeine from green tea to equal my old intake, my total caffeine intake has dropped significantly as a direct result of using the other substances found only in green tea, it appears to be correcting a central stimulant deficiency via COMT inhibition. I have lost my fanatical obsession with getting my coffee.

Wooo,I am reading your blog now while drinking my green tea.Interesting stuff and I am not a blinker.....don't know yet if thats good or bad.Felt extremely hot today....that feel good heat that generates from the gut and lifts the mood.I hope its not something you need to go off to reset the receptors.

Dam Wooo....weird you think alot like me.Its like your answering alot of the questions I have had in my head that just linger from either dumbness or laziness.

Love this post by u at your commenst about Guyanet...

"IT also bothers me that he is more and more brazenly trying to DISSUADE people from the "high insulin leads to obesity, particularly carbohydrate" idea, which is FAR more researched, supported, with oodles of personal testimony behind it.

That part is the one that pushes me from "annoyed" to "angry". No one should write a blog post as the one I quoted above. That should NEVER happen. When you discover the freedom of stable blood sugar on a carbohydrate controlled diet, an idiot should not be allowed to confuse you back into uncertainty regarding what occurred and what to do about it.""

I keep getting confused back into carb world.I eat starch and my stomach bloats out and my hypoglycemia gets worse by the day so I go back to LC.....then I read all these starch pushers and I believe them all over again....its kinda crazy!!

Guyanet is trying to dissuade people from the"high insulin from eating carbs causes obesity"thought because HE,S RIGHT.A HIGH CARB DIET DOES NOT CAUSE OBESITY, A HYPERCALORIC DIET DOES.if low carbs helps you cut calories,well so be it.IT,S NOT THE CARBS OR THE RESULTANT INSULIN SPIKE.IF IT WAS EVERY TOUR-DE FRANCE cyclist would be obese.now is where you tell me that they are burning off their carbs that,s why they don,t obese.YES CORRECT ,IN OTHER WORDS THEY ARE CONSUMING THE CORRECT AMOUNT OF CALORIES.MATTERS NOT ONE BIT THAT IT WAS CARBS.

you really think the insulin high carb theory is far more researched and supported?supported more than what?guyanet,s food reward thery?ya i agree.far more researched and supported against energy balance theroy ?I THINK NOT.

Cwaiand,I have always said that its all about the calories first.I also think that carbs actually boost the metabolism and if you are great at keeping BS stable then eat a normal diet.I do feel though that the more stable you can keep your blood glucose over a lifespan the better you will age.BS spikes age me fast....I do not know if its maybe the BS glycating or if high insulin damages the body,all I know is I notice an anti-aging effect of LCHF.Another day at 1000cal,pants are slightly looser and I am writing this with just a slight hunger pang.

I posted about Guyanet because here I am losing weight and looking good again but I like to open my mind and so visit all health sites online.That makes me start to believe that I am wrong in how I am feeling right now and starch will cure me....it always ends the same way.

i hear what your saying.it would be nice to get real facts on what to eat.i understand you eating what makes you feel better ,seems the right thing to do.i don,t know for a fact that it is the right thing to do.cocaine might make me feel better but i,m not sure if it,s good for me.

@Cwaiand*pats head*, oh little one, how many times must I reiterate? Energy balance is not mutually exclusive with carb/insulin theory. They are quite compatable.

Yes, there are a few nuts who believe only carbs raise insulin and that you have 0 insulin on low carb. Those people are either ignorant, crazy, or liars.

What we, 99% of the carb/insulin theory proponents would argue, is that carbohydrate mediated insulin surges are the catalyst behind the physiological expansion of fat tissue and subsequent hyperphagia. We would argue that energy balance is a down stream effect of insulin being too high too much of the time, and fat oxidation not occuring enough after meals.

I cannot argue with my hawk eye self observation, I can almost TIME and PREDICT how my body will react (hunger, energy) to various conditions and the common denominator is always that any condition leading to more insulin -> hunger and fatigue.

When I said it was "more researched/evidenced" I was speaking exclusively of Guyenets ridiculous food reward idea. I would never say low carb is superior to energy balance because that is like saying, medicine is superior to being totally disease free. The point of medicine is to eradicate disease. The goal is to be disease free. Medicine cannot be superior to a disease free state as a disease free state is the entire goal of medicine.

This is much in the way low carb is an eating strategy designed to reduce postprandial hyperinsulinemia, thus normalize metabolism, preent drops in FFAs and glucose, thus prevent fatty acid oxidation suppression, and subsequently reduce food intake due to maintaining a superior energized (thus low appetite) state while food deprived.

All of your talk about counting calories and JUST EAT LESS is frigging ignorant of the fact some people (i.e. fatsos like me) make way too much insulin in response to certain foods - attempting to "just count calories" is doomed to fail as I am not a masochist and cannot live my life tired and hungry due to fighting insulin surges (i.e. refusing to eat in response to drops in FFA and glucose mediated by insulin surges produced by the glucose I cannot tolerate).

so your saying you have reactive hypogycemia?you said you produce too much insulin in response to food.this would lead to blood sugar crashes.easily tested for.this talk of insulin spikes and surges is such a joke.if your eating to energy requirment then the surges and peaks of insulin are normal.inbetween these surges your body will burn fats.it switches constantly and seemlessly.you think there,s any difference in eating 2500 calories at 1 meal as oppossed to eating 2500 calories spread through out the day?if 2500 calories is energy balance then it makes no difference to your body composition.same amount of total insulin released(just in a different pattern)same fat burning.

i have no problem with low carb.the reason it works for people is not the reasons given by you or taubes or whom ever else follows his book.low carb is a very good stategy for hunger control and for CUTTING CALORIES.IT,S EFFECT ON INSULIN SURGES AND SPIKES AND TOTAL RELEASE IS ALL BUNK.

eat 80%carbs on a 2000 cal diet with little to no fat,guess what burn the carbs(body upregulates carb burning over fat burning)the diet is low in dietary fat so no fat to store.eat the same 2000 calorie diet of 80% fat no carbs ,body burns fat as no carbs are available for energy.guess what ,no fat to store as it was used for energy requirements.fat loss on such a diet would actually be higher on the high CARB diet as the energy required to burn carbs is greater.INSULIN SPIKES WON,T AFFECT THIS OUT COME.these studies have been done on humans in metabolic ward conditions.changing the macro,s of fat to carbs has NO DIFFERENCE IN FAT LOSS(SLIGHT FAVOR OF CARBS).

LOW CARB IS A CALORIE CUTTING AND APPEITITE CONTROLLING STRATEGY.IT,S NOT ABOUT THE INSULIN.

About Me

I am Petro Dobromylskyj, always known as Peter. I'm a vet, trained at the RVC, London University. I was fortunate enough to intercalate a BSc degree in physiology in to my veterinary degree. I was even more fortunate to study under Patrick Wall at UCH, who set me on course to become a veterinary anaesthetist, mostly working on acute pain control. That led to the Certificate then Diploma in Veterinary Anaesthesia and enough publications to allow me to enter the European College of Veterinary Anaesthesia and Analgesia as a de facto founding member. Anaesthesia teaches you a lot. Basic science is combined with the occasional need to act rapidly. Wrong decisions can reward you with catastrophe in seconds. Thinking is mandatory.
I stumbled on to nutrition completely by accident. Once you have been taught to think, it's hard to stop. I think about lots of things. These are some of them.

Organisation (or lack of it)!

The "labels" function on this blog has been used to function as an index and I've tended to group similar subjects together by using labels starting with identical text. If they're numbered within a similar label, start with (1). The archive is predominantly to show the posts I've put up in the last month, if people want to keep track of recent goings on. I might change it to the previous week if I ever get to time to put up enough posts in a week to justify it. That seems to be the best I can do within the limits of this blogging software!